Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation
Abstract Aims This study aimed to determine whether ( a ) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); ( b ) with the dura...
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| Veröffentlicht in: | The American journal of emergency medicine 2012-09, Vol.30 (7), p.1202-1209 |
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| creator | Li, Jing-sha, MD Zhong, Jing-quan, MD, PhD Liu, Hong-zhen, MD Zeng, Qi-xian, MD Meng, Xiang-lin, MD Liu, Dong-lin, MD Su, Guo-ying, MD Zhang, Yun, MD, PhD |
| description | Abstract Aims This study aimed to determine whether ( a ) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); ( b ) with the duration of VF, the degree of the imbalance would be greater; and ( c ) there was a relationship between the level of MMP-9 or TIMP-1 and the cardiac function. Methods and Results Ventricular fibrillation was electrically induced in 24 dogs. The animals were randomly divided into 3 groups (sham control, n = 8; 8-minute VF, n = 8; 12-minute VF, n = 8). Echocardiographic measurement and hemodynamic variables were recorded before VF and after return of spontaneous circulation. Tissue inhibitor of metalloproteinase 1 (TIMP-1) and MMP-9 were analyzed by Western blot and immunohistochemistry. Compared with sham controls, dogs under VF and CPR showed significantly decreased level of TIMP-1 ( P < .001), and with the duration of VF, the level of TIMP-1 declined ( P < .01). The level of MMP-9 did not achieve statistical significance in the 3 groups ( P > .05); however, they were higher in VF and longer duration VF groups. The ratios of TIMP-1/MMP-9 were lower in VF groups ( P < .05). There was a negative correlation between TIMP-1 and left atrium dimension and left ventricular diastolic dimensions ( r = −0.83 and r = −0.96, respectively; P < .01) and a positive correlation between TIMP-1 and left ventricular ejection fraction ( r = 0.85; P < .01). Conclusions There was an imbalance between TIMP-1 and MMP-9 after CPR. It may partly contribute to the postresuscitation cardiac dysfunction. |
| doi_str_mv | 10.1016/j.ajem.2011.07.006 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1035528475</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0735675711003238</els_id><sourcerecordid>2746904621</sourcerecordid><originalsourceid>FETCH-LOGICAL-c469t-4eb95410b4f922237af61e6c34318dab0ac5350c4f19cac7d813906d27316ec73</originalsourceid><addsrcrecordid>eNp9kl2L1TAQhoMo7nH1D3ghARG8aZ0kTdKCCLL4sbDghXod0nSKObbNMUnVBX-8KefowiJe5SLPTN6ZJ4Q8ZlAzYOrFvrZ7nGsOjNWgawB1h-yYFLxqmWZ3yQ60kJXSUp-RByntoYCNbO6TM85BAAfYkV-Xc28nuzikPeYfiAvNPqUVqV---N7nEGkY6YzZTlM4xJDRLzYhZdQuA51tjv7nP647aseMkTobBx8O6zSHxcZrGjGtyflssw_LQ3JvtFPCR6fznHx---bTxfvq6sO7y4vXV5VrVJerBvtONgz6Zuw450LbUTFUTjSCtYPtwTopJLhmZJ2zTg8tEx2ogWvBFDotzsnzY98S8NuKKZvZJ4dTmRvDmgwDISVvGy0L-vQWug9rXEq6IyVbobaG_Ei5GFKKOJpD9HOZr0Bmc2P2ZnNjNjcGtCluStGTU-u1n3H4W_JHRgGenQCbnJ3GWLT4dMMpwSW0W8aXRw7Lzr57jKZsFIvCwUd02QzB_z_Hq1vlbvKLLy9-xWtMN_OaxA2Yj9sv2j4RYyUjF634DUkQwuM</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1035558367</pqid></control><display><type>article</type><title>Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Li, Jing-sha, MD ; Zhong, Jing-quan, MD, PhD ; Liu, Hong-zhen, MD ; Zeng, Qi-xian, MD ; Meng, Xiang-lin, MD ; Liu, Dong-lin, MD ; Su, Guo-ying, MD ; Zhang, Yun, MD, PhD</creator><creatorcontrib>Li, Jing-sha, MD ; Zhong, Jing-quan, MD, PhD ; Liu, Hong-zhen, MD ; Zeng, Qi-xian, MD ; Meng, Xiang-lin, MD ; Liu, Dong-lin, MD ; Su, Guo-ying, MD ; Zhang, Yun, MD, PhD</creatorcontrib><description>Abstract Aims This study aimed to determine whether ( a ) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); ( b ) with the duration of VF, the degree of the imbalance would be greater; and ( c ) there was a relationship between the level of MMP-9 or TIMP-1 and the cardiac function. Methods and Results Ventricular fibrillation was electrically induced in 24 dogs. The animals were randomly divided into 3 groups (sham control, n = 8; 8-minute VF, n = 8; 12-minute VF, n = 8). Echocardiographic measurement and hemodynamic variables were recorded before VF and after return of spontaneous circulation. Tissue inhibitor of metalloproteinase 1 (TIMP-1) and MMP-9 were analyzed by Western blot and immunohistochemistry. Compared with sham controls, dogs under VF and CPR showed significantly decreased level of TIMP-1 ( P < .001), and with the duration of VF, the level of TIMP-1 declined ( P < .01). The level of MMP-9 did not achieve statistical significance in the 3 groups ( P > .05); however, they were higher in VF and longer duration VF groups. The ratios of TIMP-1/MMP-9 were lower in VF groups ( P < .05). There was a negative correlation between TIMP-1 and left atrium dimension and left ventricular diastolic dimensions ( r = −0.83 and r = −0.96, respectively; P < .01) and a positive correlation between TIMP-1 and left ventricular ejection fraction ( r = 0.85; P < .01). Conclusions There was an imbalance between TIMP-1 and MMP-9 after CPR. It may partly contribute to the postresuscitation cardiac dysfunction.</description><identifier>ISSN: 0735-6757</identifier><identifier>EISSN: 1532-8171</identifier><identifier>DOI: 10.1016/j.ajem.2011.07.006</identifier><identifier>PMID: 22030200</identifier><identifier>CODEN: AJEMEN</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Blotting, Western ; Cardiopulmonary Resuscitation ; Chronic illnesses ; CPR ; Cytokines ; Disease Models, Animal ; Dogs ; Emergency ; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care ; Emergency medical care ; Female ; Heart - physiopathology ; Heart attacks ; Intensive care medicine ; Ischemia ; Male ; Matrix Metalloproteinase 9 - blood ; Matrix Metalloproteinase 9 - physiology ; Medical sciences ; Rodents ; Studies ; Time Factors ; Tissue Inhibitor of Metalloproteinase-1 - blood ; Tissue Inhibitor of Metalloproteinase-1 - physiology ; Ventricular Fibrillation - blood ; Ventricular Fibrillation - physiopathology ; Ventricular Fibrillation - therapy</subject><ispartof>The American journal of emergency medicine, 2012-09, Vol.30 (7), p.1202-1209</ispartof><rights>Elsevier Inc.</rights><rights>2012 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-4eb95410b4f922237af61e6c34318dab0ac5350c4f19cac7d813906d27316ec73</citedby><cites>FETCH-LOGICAL-c469t-4eb95410b4f922237af61e6c34318dab0ac5350c4f19cac7d813906d27316ec73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0735675711003238$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26325085$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22030200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Jing-sha, MD</creatorcontrib><creatorcontrib>Zhong, Jing-quan, MD, PhD</creatorcontrib><creatorcontrib>Liu, Hong-zhen, MD</creatorcontrib><creatorcontrib>Zeng, Qi-xian, MD</creatorcontrib><creatorcontrib>Meng, Xiang-lin, MD</creatorcontrib><creatorcontrib>Liu, Dong-lin, MD</creatorcontrib><creatorcontrib>Su, Guo-ying, MD</creatorcontrib><creatorcontrib>Zhang, Yun, MD, PhD</creatorcontrib><title>Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation</title><title>The American journal of emergency medicine</title><addtitle>Am J Emerg Med</addtitle><description>Abstract Aims This study aimed to determine whether ( a ) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); ( b ) with the duration of VF, the degree of the imbalance would be greater; and ( c ) there was a relationship between the level of MMP-9 or TIMP-1 and the cardiac function. Methods and Results Ventricular fibrillation was electrically induced in 24 dogs. The animals were randomly divided into 3 groups (sham control, n = 8; 8-minute VF, n = 8; 12-minute VF, n = 8). Echocardiographic measurement and hemodynamic variables were recorded before VF and after return of spontaneous circulation. Tissue inhibitor of metalloproteinase 1 (TIMP-1) and MMP-9 were analyzed by Western blot and immunohistochemistry. Compared with sham controls, dogs under VF and CPR showed significantly decreased level of TIMP-1 ( P < .001), and with the duration of VF, the level of TIMP-1 declined ( P < .01). The level of MMP-9 did not achieve statistical significance in the 3 groups ( P > .05); however, they were higher in VF and longer duration VF groups. The ratios of TIMP-1/MMP-9 were lower in VF groups ( P < .05). There was a negative correlation between TIMP-1 and left atrium dimension and left ventricular diastolic dimensions ( r = −0.83 and r = −0.96, respectively; P < .01) and a positive correlation between TIMP-1 and left ventricular ejection fraction ( r = 0.85; P < .01). Conclusions There was an imbalance between TIMP-1 and MMP-9 after CPR. It may partly contribute to the postresuscitation cardiac dysfunction.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cardiopulmonary Resuscitation</subject><subject>Chronic illnesses</subject><subject>CPR</subject><subject>Cytokines</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>Emergency</subject><subject>Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care</subject><subject>Emergency medical care</subject><subject>Female</subject><subject>Heart - physiopathology</subject><subject>Heart attacks</subject><subject>Intensive care medicine</subject><subject>Ischemia</subject><subject>Male</subject><subject>Matrix Metalloproteinase 9 - blood</subject><subject>Matrix Metalloproteinase 9 - physiology</subject><subject>Medical sciences</subject><subject>Rodents</subject><subject>Studies</subject><subject>Time Factors</subject><subject>Tissue Inhibitor of Metalloproteinase-1 - blood</subject><subject>Tissue Inhibitor of Metalloproteinase-1 - physiology</subject><subject>Ventricular Fibrillation - blood</subject><subject>Ventricular Fibrillation - physiopathology</subject><subject>Ventricular Fibrillation - therapy</subject><issn>0735-6757</issn><issn>1532-8171</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kl2L1TAQhoMo7nH1D3ghARG8aZ0kTdKCCLL4sbDghXod0nSKObbNMUnVBX-8KefowiJe5SLPTN6ZJ4Q8ZlAzYOrFvrZ7nGsOjNWgawB1h-yYFLxqmWZ3yQ60kJXSUp-RByntoYCNbO6TM85BAAfYkV-Xc28nuzikPeYfiAvNPqUVqV---N7nEGkY6YzZTlM4xJDRLzYhZdQuA51tjv7nP647aseMkTobBx8O6zSHxcZrGjGtyflssw_LQ3JvtFPCR6fznHx---bTxfvq6sO7y4vXV5VrVJerBvtONgz6Zuw450LbUTFUTjSCtYPtwTopJLhmZJ2zTg8tEx2ogWvBFDotzsnzY98S8NuKKZvZJ4dTmRvDmgwDISVvGy0L-vQWug9rXEq6IyVbobaG_Ei5GFKKOJpD9HOZr0Bmc2P2ZnNjNjcGtCluStGTU-u1n3H4W_JHRgGenQCbnJ3GWLT4dMMpwSW0W8aXRw7Lzr57jKZsFIvCwUd02QzB_z_Hq1vlbvKLLy9-xWtMN_OaxA2Yj9sv2j4RYyUjF634DUkQwuM</recordid><startdate>20120901</startdate><enddate>20120901</enddate><creator>Li, Jing-sha, MD</creator><creator>Zhong, Jing-quan, MD, PhD</creator><creator>Liu, Hong-zhen, MD</creator><creator>Zeng, Qi-xian, MD</creator><creator>Meng, Xiang-lin, MD</creator><creator>Liu, Dong-lin, MD</creator><creator>Su, Guo-ying, MD</creator><creator>Zhang, Yun, MD, PhD</creator><general>Elsevier Inc</general><general>Elsevier</general><general>Elsevier Limited</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20120901</creationdate><title>Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation</title><author>Li, Jing-sha, MD ; Zhong, Jing-quan, MD, PhD ; Liu, Hong-zhen, MD ; Zeng, Qi-xian, MD ; Meng, Xiang-lin, MD ; Liu, Dong-lin, MD ; Su, Guo-ying, MD ; Zhang, Yun, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c469t-4eb95410b4f922237af61e6c34318dab0ac5350c4f19cac7d813906d27316ec73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cardiopulmonary Resuscitation</topic><topic>Chronic illnesses</topic><topic>CPR</topic><topic>Cytokines</topic><topic>Disease Models, Animal</topic><topic>Dogs</topic><topic>Emergency</topic><topic>Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care</topic><topic>Emergency medical care</topic><topic>Female</topic><topic>Heart - physiopathology</topic><topic>Heart attacks</topic><topic>Intensive care medicine</topic><topic>Ischemia</topic><topic>Male</topic><topic>Matrix Metalloproteinase 9 - blood</topic><topic>Matrix Metalloproteinase 9 - physiology</topic><topic>Medical sciences</topic><topic>Rodents</topic><topic>Studies</topic><topic>Time Factors</topic><topic>Tissue Inhibitor of Metalloproteinase-1 - blood</topic><topic>Tissue Inhibitor of Metalloproteinase-1 - physiology</topic><topic>Ventricular Fibrillation - blood</topic><topic>Ventricular Fibrillation - physiopathology</topic><topic>Ventricular Fibrillation - therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Jing-sha, MD</creatorcontrib><creatorcontrib>Zhong, Jing-quan, MD, PhD</creatorcontrib><creatorcontrib>Liu, Hong-zhen, MD</creatorcontrib><creatorcontrib>Zeng, Qi-xian, MD</creatorcontrib><creatorcontrib>Meng, Xiang-lin, MD</creatorcontrib><creatorcontrib>Liu, Dong-lin, MD</creatorcontrib><creatorcontrib>Su, Guo-ying, MD</creatorcontrib><creatorcontrib>Zhang, Yun, MD, PhD</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>The American journal of emergency medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Jing-sha, MD</au><au>Zhong, Jing-quan, MD, PhD</au><au>Liu, Hong-zhen, MD</au><au>Zeng, Qi-xian, MD</au><au>Meng, Xiang-lin, MD</au><au>Liu, Dong-lin, MD</au><au>Su, Guo-ying, MD</au><au>Zhang, Yun, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation</atitle><jtitle>The American journal of emergency medicine</jtitle><addtitle>Am J Emerg Med</addtitle><date>2012-09-01</date><risdate>2012</risdate><volume>30</volume><issue>7</issue><spage>1202</spage><epage>1209</epage><pages>1202-1209</pages><issn>0735-6757</issn><eissn>1532-8171</eissn><coden>AJEMEN</coden><abstract>Abstract Aims This study aimed to determine whether ( a ) there was an imbalance between matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) after cardiopulmonary resuscitation (CPR) in a canine model of prolonged ventricular fibrillation (VF); ( b ) with the duration of VF, the degree of the imbalance would be greater; and ( c ) there was a relationship between the level of MMP-9 or TIMP-1 and the cardiac function. Methods and Results Ventricular fibrillation was electrically induced in 24 dogs. The animals were randomly divided into 3 groups (sham control, n = 8; 8-minute VF, n = 8; 12-minute VF, n = 8). Echocardiographic measurement and hemodynamic variables were recorded before VF and after return of spontaneous circulation. Tissue inhibitor of metalloproteinase 1 (TIMP-1) and MMP-9 were analyzed by Western blot and immunohistochemistry. Compared with sham controls, dogs under VF and CPR showed significantly decreased level of TIMP-1 ( P < .001), and with the duration of VF, the level of TIMP-1 declined ( P < .01). The level of MMP-9 did not achieve statistical significance in the 3 groups ( P > .05); however, they were higher in VF and longer duration VF groups. The ratios of TIMP-1/MMP-9 were lower in VF groups ( P < .05). There was a negative correlation between TIMP-1 and left atrium dimension and left ventricular diastolic dimensions ( r = −0.83 and r = −0.96, respectively; P < .01) and a positive correlation between TIMP-1 and left ventricular ejection fraction ( r = 0.85; P < .01). Conclusions There was an imbalance between TIMP-1 and MMP-9 after CPR. It may partly contribute to the postresuscitation cardiac dysfunction.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>22030200</pmid><doi>10.1016/j.ajem.2011.07.006</doi><tpages>8</tpages></addata></record> |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Blotting, Western Cardiopulmonary Resuscitation Chronic illnesses CPR Cytokines Disease Models, Animal Dogs Emergency Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care Emergency medical care Female Heart - physiopathology Heart attacks Intensive care medicine Ischemia Male Matrix Metalloproteinase 9 - blood Matrix Metalloproteinase 9 - physiology Medical sciences Rodents Studies Time Factors Tissue Inhibitor of Metalloproteinase-1 - blood Tissue Inhibitor of Metalloproteinase-1 - physiology Ventricular Fibrillation - blood Ventricular Fibrillation - physiopathology Ventricular Fibrillation - therapy |
| title | Imbalance between tissue inhibitor of metalloproteinase 1 and matrix metalloproteinase 9 after cardiopulmonary resuscitation |
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